Decreased systemic formation of prostaglandin E and prostacyclin, and unchanged thromboxane formation, in alcoholics during withdrawal as estimated from metabolites in urine

1. The rates of secretion into the circulation of prostaglandin E, prostacyclin, and thromboxane A2 were estimated in male alcoholics on the third day of withdrawal and in control subjects by measuring appropriate metabolites in urine. 2. Urinary levels of tetranor-5,11-diketo-7α-hydroxyprostane-1,16-dioic acid (the major urinary metabolite of prostaglandins E1 and E2), of 2,3-dinor-6-ketoprostaglandin F1α (the major urinary metabolite of prostacyclin) and of 6-keto-prostaglandin F1α (the stable hydrolysis product of prostacyclin) were significantly different from the normal subjects in the alcoholic group. In contrast, 2,3-dinor-thromboxane B2 (the major urinary metabolite of thromboxane A2) and thromboxane B2 (the stable hydrolysis product of thromboxane A2) were not significantly different between the groups. 3. These data suggest that the ratio of the vasodilator prostanoids prostaglandin E and prostacyclin and the vasoconstrictor prostanoid thromboxane A2 is lower than in normal subjects, in alcoholics during withdrawal. This may be one causal factor for the higher incidence of hypertension observed in withdrawing alcoholics compared with control subjects.

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Dexamethasone effect on prostanoid formation in healthy man

Clinical Science ◽

10.1042/cs0680681 ◽

1985 ◽

Vol 68 (6) ◽

pp. 681-685 ◽

Cited By ~ 21

Author(s):

Bernd Rosenkrantz ◽

Aniko Náray-Fejes-Tóth ◽

Geza Fejes-Tóth ◽

Christine Fischer ◽

Masafumi Sawada ◽

...

Keyword(s):

Thromboxane B2 ◽

Urinary Metabolite ◽

Dioic Acid ◽

Healthy Man ◽

Major Urinary Metabolite ◽

Healthy Female ◽

Total Body ◽

Prostaglandins E1 And E2 ◽

Platelet Thromboxane ◽

Thromboxane Formation

1. Dexamethasone was administered to six healthy female volunteers for 4 days, resulting in plasma levels of 4.8 ± 1.4 × 10−8 mol/l. Urinary excretions of six prostanoids as well as collagen-induced platelet thromboxane formation and aggregation were determined before, during and 1 month after administration of dexamethasone. 2. Dexamethasone had no effect on urinary thromboxane B2 (77 ± 22 ng/day vs 63 ± 16 ng/day during dexamethasone), dinor-thromboxane B2, the major urinary metabolite of thromboxane B2 (406 ± 84 ng/day vs 380 ± 90 ng/day), dinor-6-keto-prostaglandin F1α, the major urinary metabolite of prostacyclin (199 ± 41 ng/day vs 237 ± 53 ng/day), tetranor-5,1 l-diketo-7α-hydroxy-prostane-1,16-dioic acid, the major urinary metabolite of prostaglandins E1 and E2 (7712 ± 1677 ng/day vs 7886 ± 2565 ng/day) and tetranor-11-keto-5α, 7α-dihydroxy-prostane-1,16-dioic acid, the major urinary metabolite of prostaglandins F1α and F2α (14 394 ± 2053 ng/day vs 18288 ± 2251 ng/day). Prostaglandin E2 excretion slightly but significantly increased from 217 ± 48 ng/day to 294 ± 55 ng/day. Collagen-induced platelet thromboxane formation and aggregation were not altered. 3. These results suggest that glucocorticoids do not regulate renal, platelet or total body prostanoid formation in healthy man.

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Prostaglandin E-Major Urinary Metabolite (PGE-MUM) as a Tumor Marker for Lung Adenocarcinoma

Cancers ◽

10.3390/cancers11060768 ◽

2019 ◽

Vol 11 (6) ◽

pp. 768 ◽

Cited By ~ 1

Author(s):

Hironori Kawamoto ◽

Hiromichi Hara ◽

Jun Araya ◽

Akihiro Ichikawa ◽

Yu Fujita ◽

...

Keyword(s):

Lung Adenocarcinoma ◽

Cancer Progression ◽

Stage Iv ◽

Staging System ◽

Tnm Staging ◽

Tumor Burden ◽

Urinary Metabolite ◽

Prostaglandin E ◽

Major Urinary Metabolite ◽

Embryonic Antigen

Background: Prostaglandin E2 (PGE2) is metabolized to prostaglandin E-major urinary metabolite (PGE-MUM). Enhanced cyclooxygenase-2 (COX-2) expression demonstrated in lung adenocarcinoma indicates increased PGE-MUM levels in patients with lung adenocarcinoma. Objectives: We aimed to elucidate the clinical usefulness of measuring PGE-MUM as an indicator of tumor burden in patients with lung adenocarcinoma. Methods: PGE-MUM was measured by a radioimmunoassay in control healthy volunteers (n = 124) and patients with lung adenocarcinoma (n = 54). Associations between PGE-MUM levels and clinical characteristics of the patients (including lung cancer stage and TNM factors (T: Tumor, N: Node, M: Metastasis) were examined. Results: PGE-MUM levels were significantly elevated in patients with lung adenocarcinoma. A PGE-MUM level of 14.9 μg/g∙Cr showed 70.4% sensitivity and 67.7% specificity for the diagnosis of lung adenocarcinoma. PGE-MUM levels tended to be positively correlated with cancer progression as determined by the TNM staging system. Advanced stage (stage III, stage IV, and recurrence) was significantly associated with high PGE-MUM levels by logistic regression analysis. No apparent correlation was demonstrated between PGE-MUM and carcinoma embryonic antigen (CEA) levels. Conclusions: PGE-MUM can be a promising biomarker reflecting the systemic tumor burden of lung adenocarcinoma.

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